NEET MDS Lessons
General Pathology
EMBOLISM
Definition: transportation of an abnormal mass of an abnormal mass of undissolved material from one part of circulation to another. The mass transported is called embolus.
Types
I .Thrombi and clots.
2. Gas or air.
3. Fat
4.Amniotic fluid.
5.Tumour
Thromboembolism
This is the commonest type of embolus and may be formed of the primary thrombus or more often of propagated clot region which is loosely attached.
Emboli from venous thrombi can result In impaction in the pulmonary arteries and result in sudden death.
Embolism from cardiac or arterial thrombi results in systemic embolism causing infraction and gangrene.
Gaseous
This occurs when gas is introduced into the circulation:
• Accidental opening of large veins during surgery.
• Mismanaged transfusion. .
As air is readily absorbed into blood only sudden introduction or large quantities of air produces effects
Caisson’s Disease bubbling of nitrogen from the blood during sudden decompression as seen during deep sea diving.
Fat Embolism
Causes
• Fractures especially of long bones and multiple
• Crush injuries.
Sites of impaction:
o Lungs.
o Systemic: causing -
→ petechial skin haemorrhages.
→ Embolism to brain leading to coma and death.
→ Conjunctival and retinal haemorrhages
Tumor Embolism.
Invasion of vascular channe1.s is a feature of malignant neoplasms and this leads to:
• Metastatic deposits,
• DlC
Osteonecrosis (Avascular Necrosis)
Ischemic necrosis with resultant bone infarction occurs mostly due to fracture or after corticosteroid use. Microscopically, dead bon trabevulae (characterized by empty lacunae) are interspersed with areas of fat necrosis.
The cortex is usually not affected because of collateral blood supply; in subchondral infarcts, the overlying articular cartilage also remains viable because the synovial fluid can provide nutritional support. With time, osteoclasts can resorb many of the necrotic bony trabeculae; any dead bone fragments that remain act as scaffolds for new bone formation, a process called creeping substitution.
Symptoms depend on the size and location of injury. Subchondral infarcts often collapse and can lead to severe osteoarthritis.
Iron deficiency anaemia.
Absorption of iron is affected by :
- Iron stores.
- Rate of erythropoiesis
- Acid pH aids absorption.
- Phosphates and phytates in diet impair absorption.
Causes of deficiency:
- Increased demand:
o Growth (in children)
o Menstruation, Pregnancy, lactation.
- Inadequate intake and absorption.
o Dietary deficiency.
o Achlorhydria or gastrectomy.
o Malabsorption states.
- Chronic blood loss
o Peptic ulcer, bleeding piles
o Menorrhagia.
o Hook worm infestation
Features:
- Anaemia.
- Koilonychia.
- Atrophic glossitis and angular stomatitis.
- Dysphagia-Plummer Vinson syndrome.
Blood findings:
- Microcytjc_hypochromic cells, ring cells and pessary cells.
- Anisocytosis and poikilocytosis.
- Low MCV. MCH and MCHC.
- Serum iron is low but iron binding capacity is increased
Bone marrow
Erythroid hyperplasia with imcronormoblasts. Iron stains reveal depleted stores
Differential diagnosis .-
- Sideroblastic anaemia which is also microcytic hypochromic but there is excess iron in the erythroid cells .Some are pyridoxine responsive.
- (ii) Thalassaemia
HYPERPLASIA
It is the increase in the size of an organ or tissue due to increase in the number of its constituent cells. This is seen in organs made up of labile and stable cells.
Causes
I. Increased demand:
- Bone marrow in hypoxia and haemolytic states.
- Thyroid gland in puberty
2. Persistant Trauma:
- Acanthosis of the epidermis in chronic inflammations and in warts.
- Hyperplasia of oral mucosa due tooth and denture trauma.
- Mucosa at the edges of a gastric ulcer.
3. Endocrine target organ:
- Pregnancy hyperplasia of breast.
- Prostatic hyperplasia.
4. Compensatory:
Hyperplasia of kidney when the other kidney has been removed.
5. Idiopathic:
Endocrine organs like thyroid, adrenals, pituitary etc. can undergo hyperplasia with no detectable stimulus. .
Cytopathologic techniques
Cytopathology is the study of cells from various body sites to determine the cause or nature of disease.
Applications of cytopathology:
- Screening for the early detection of asymptomatic cancer
2. Diagnosis of symptomatic cancer
3. Surveillance of patients treated for cancer
Cytopathologic methods
There are different cytopathologic methods including:
1. Fine-needle aspiration cytology (FNAC) -In FNAC, cells are obtained by aspirating the diseased organ using a very thin needle under negative pressure.
Superficial organs (e.g. thyroid, breast, lymph nodes, skin and soft tissues) can be easily aspirated.
Deep organs, such as the lung, mediastinum, liver, pancreas, kidney, adrenal gland, and retroperitoneum are aspirated with guidance by fluoroscopy, ultrasound or CT scan.
- Exfoliative cytology
Refers to the examination of cells that are shed spontaneously into body fluids or secretions. Examples include sputum, cerebrospinal fluid, urine, effusions in body cavities (pleura, pericardium, peritoneum), nipple discharge and vaginal discharge.
- Abrasive cytology
Refers to methods by which cells are dislodged by various tools from body surfaces (skin, mucous membranes, and serous membranes). E.g. preparation of cervical smears with a spatula or a small brush to detect cancer of the uterine cervix at early stages.
Acanthosis nigricans is a pigmented skin lesion commonly present in the axilla which is a phenotypic marker for an insulin-receptor abnormality as well as a marker for adenocarcinoma, most commonly of gastric origin.
Glycogen storage diseases (glycogenoses)
1. Genetic transmission: autosomal recessive.
2. This group of diseases is characterized by a deficiency of a particular enzyme involved in either glycogen production or degradative pathways.
Diseases include:
on Gierke disease (type I)
(a) Deficient enzyme: glucose-6-phosphatase.
(b) Major organ affected by the buildup of glycogen: liver.
Pompe disease (type II)
(1) Deficient enzyme: α-glucosidase(acid maltase).
(2) Major organ affected by the buildup of glycogen: heart.
Cori disease (type III)
(1) Deficient enzyme: debranching enzyme (amylo-1,6-glucosidase).
(2) Organs affected by the buildup of glycogen: varies between the heart, liver, or skeletal muscle.
Brancher glycogenosis (type IV)
(1) Deficient enzyme: branching enzyme.
(2) Organs affected by the buildup of glycogen: liver, heart, skeletal muscle, and brain.
McArdle syndrome (type V)
(1) Deficient enzyme: muscle phosphorylase.
(2) Major organ affected by the buildup of glycogen: skeletal muscle.